Oxidative Stress and Brain Disorders
For years researchers have known that free radicals can cause cell degeneration, especially in the brain. Scientists have implicated the unstable molecules as a cause of neurodegenerative disorders such as Lou Gehrig's disease, Parkinson's disease and Huntington's disease. Now researchers are unraveling the pathways of free radical destruction in order to create targeted therapies for these disorders.
Apples brown. Butter turns rancid. Iron rusts. All are everyday signs of oxidative stress, destruction caused by free radical molecules. But none of these nuisances compare to what these unstable molecules can do inside the body, especially to cells of the brain.
Free radicals, which are products of normal cell processes, wreak havoc during their hunt for a mate. The source of their devastating actions is this oxygen molecule's unpaired electron which makes it unstable and electrically charged. It becomes stable by interacting with the nearest available molecule. Having no prejudices, it targets proteins, fats, or even DNA. Scientists have discovered that the free radical's actions can damage molecules they react with and sometimes cause the cell's demise.
Scientists are now trying to stop free radical mayhem by studying the various roads the molecule takes when it corrodes the cells of the brain.
This research is leading to:
Greater understanding of how nerve cell death occurs. Therapies to head off the destructive journey of the free radical and potentially stop nerve cell death in neurological disorders.
Under normal circumstances the body is not surprised by the free radical's intrusion and readily disarms it. Since the 1960s, scientists have known that these molecules permeate the environment as reaction by-products of substances such as oxygen, smog and cigarette smoke. Each cell in our body produces billions a day through common reactions such as turning food into energy.
While an apple may not be able to resist the assault, humans are equipped with a series of defenses, or antioxidants, that control free radical molecules and mend damage. For example, the enzyme superoxide dismutase (SOD) helps to detoxify certain harmful free radicals. Free radical scavengers such as Vitamin E mop up free radicals and help prevent damage to critical cell structures.
Other evidence suggests that ailments characterized by a loss of neurons, such as Parkinson's disease, Lou Gehrig's disease, and Huntington's disease may result from an imbalance in free radical production and internal defenses. Researchers speculate that age, abnormal stress, or genetic defects in the body's defense system corrupts internal checks and balances to reinforce the free radical reign causing cell damage.
Researchers discovered that the neurotransmitter glutamate plays a role in the neurodegenerative pathway. They believe that accumulation of glutamate and related amino acids in the brain trigger oxidative stress and neurotoxicity in Huntington's disease and amyotrophic lateral sclerosis, known as ALS or Lou Gehrig's disease.
A recently approved therapy, riluzole, puts glutamate out of commission. Two studies of more than 1,100 patients with a form of ALS showed the drug could prolong life an average of three months.
Scientists' efforts to dissect the free radical pathway also led them recently to discover the activation of the survival gene, bcl-2, can protect nerve cells from the cell death signals induced by free radicals. One form of ALS may result from defects in the gene responsible for producing the neuro-protector, SOD. Studies performed in yeast show that the activation of the bcl-2 gene stops free radical induced death in cells lacking a functional SOD gene. A potential therapeutic treatment could involve increasing expression of the bcl-2 gene in patients, thereby increasing nerve cell survival.
The hope is that further deciphering of the free radical pathway will continue to lead to new therapies. Future treatments may involve a "cocktail" of mixtures that target various points along the free radical pathway and stop nerve cell death.
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